June 3, 2020

NGM Biopharmaceuticals, Inc.

C o r p o r a t e O v e r v i e w

J u n e 2 0 2 0

Novel Biology.

Powerful Medicines.

Transformative Impact.

NASDAQ: NGM

2

Safe Harbor Statement

This presentation contains forward-looking statements, including, but not limited to, statements regarding potential indications for, and planned development of, product candidates in NGM’s pipeline, including aldafermin; the planned timing of initiation, enrollment and results of NGM’s clinical trials; the potential activity, complementarity, safety, tolerability and efficacy of NGM’s product candidates, including aldafermin and specifically including its differentiation and the potential benefits of extended treatment with aldafermin; NGM’s option to participate in the economic return of any programs licensed by our collaborator, Merck; NGM’s expectation of potential value-driving catalysts and the timing thereof; and any other statements other than statements of historical facts. Because such statements deal with future events and are based on NGM’s current plans, objectives, estimates and expectations, they are subject to various significant risks and uncertainties and actual results, performance and achievements and the timing of events could differ materially from those described in or implied by the statements herein. Such risks and uncertainties include, without limitation, those associated with the costly and time-consuming pharmaceutical product development process and the uncertainty of clinical success, including risk related to failures or delays in successfully initiating, enrolling or completing clinical trials; the risk that results obtained in NGM’s clinical trials to date may not be indicative of results obtained in ongoing or future trials, including pivotal trials, including the risk that ongoing or future studies show that aldafermin is not a tolerable or effective treatment for NASH patients; the COVID-19 pandemic, which may significantly impact (i) our business and operations, including out of our headquarters in the San Francisco Bay Area and our clinical trial sites, as well as the business or operations of our manufacturers, contract research organizations or other third parties with whom we conduct business, (ii) our ability to access capital, (iii) the value of our common stock and (iv) the future decisions of our collaborator; the time-consuming and uncertain regulatory approval process; seeking and maintaining protection of intellectual property; NGM’s reliance on third party manufacturers and delays or problems in the manufacture of product candidates; the sufficiency of NGM’s cash resources and need for additional capital; and other risks and uncertainties affecting NGM and its research and development programs, including those described under the caption "Risk Factors" and elsewhere in NGM’s quarterly report on Form 10-Q for the quarter ended March 31, 2020 and future filings and reports of NGM with the Securities and Exchange Commission. The forward-looking statements contained herein are made only as of the date hereof or as of the dates indicated in the forward-looking statements, even if they are subsequently made available by NGM on its website or otherwise. NGM undertakes no obligation to update or supplement any forward-looking statements after the date hereof, or to update the reasons why actual results may differ or differ materially from those anticipated in the forward-looking statements.

June 3, 2020

Company Highlights

3

Experienced team

with highly

productive R&D

engine generating

on average

1 development

candidate/year

Pipeline of three

additional ongoing

clinical-stage

product candidates

in cardio-metabolic,

oncologic and

ophthalmic diseases

Strategic

collaboration with

Merck –

up to $75M/yr. R&D

support1

and NGM option

on future Merck

late-stage programs

Multiple key

milestones and

potential value-

driving catalysts

expected in the next

12-18 months

Aldafermin

(NGM282)

Wholly-owned,

Phase 2b product

candidate for

treatment of NASH

NGM313

(MK-3655)

Insulin sensitizer

for treatment of

NASH and T2D;

Licensed by Merck

1 Merck has committed to provide R&D reimbursement of up to $50 million per year. If our R&D expenses exceed $50 million in a given year, Merck can either reimburse up to an additional $25 million for use in funding IND-enabling or later-staged activities or provide us with the equivalent value in in-kind services for such activities.NASH: non-alcoholic steatohepatitisT2D: type 2 diabetes

June 3, 2020

OngoingDevelopment

Programs

5

Our Expansive Pipeline

4

PRODUCTCANDIDATE

PRODUCT DESCRIPTION(DOSING FREQUENCY)

POTENTIALINDICATIONS

STAGE OF DEVELOPMENT

WORLDWIDECOMMERCIAL RIGHTS

Aldafermin(NGM282)

FGF19 Analog(Once Daily)

NASH

NGM313(MK-3655)

FGFR1c/KLB Agonistic Antibody(Once Monthly)

NASH, Type 2 Diabetes

NGM120GFRAL Antagonistic Antibody

(Long Acting)

Cancer,Cancer Anorexia/Cachexia

Syndrome (CACS)

NGM621Complement C3 Inhibitory

Antibody(Long Acting)

Dry AMD / Geographic Atrophy

NGM395GDF15 Analog(Long Acting)

Metabolic

Option

Option

Wholly-OwnedPhase 2b

Phase 1b

Phase 1a/1b

Phase 1

Licensed

FGF19: fibroblast growth factor 19; FGFR1c/KLB: fibroblast growth factor receptor 1c/beta-klotho; GFRAL: glial-cell-derived neurotrophic factor receptor alpha-like; GDF15: growth differentiation factor 15

Wholly-Owned

Phase 1

June 3, 2020

Target Population

Fibrosis Stage

U.S. Prevalence (Millions) 3.5 6.3 3.4 2.0 1.3

Drivers of Mortality

Time to Progression Approximately One Fibrosis Stage Worsening Every 7 Years

Improving Fibrosis Leads to Better Outcomes for NASH Patients

5Sources: Dulai et al, Hepatology 2017, 65(5):1557-1565; Singh et al, Clin Gastroenterol Hepatol. 2015, 13(4): 643–654; Estes et al, Hepatology 2018, 67(1): 123-133. 1 H Razavi, Paris NASH meeting July 5, 2018 presentation ”The value proposition of NASH therapy on the burden of disease related to obesity”

Liver-related Mortality Rates

(per 1,000 Patients)

F0 F1 F2 F3 F4

Cardiovascular Disease Liver Disease

No / Early Fibrosis

Exponential increase in liver-related mortality

All-cause mortality dominated by

cardiovascular complications

Decompensated cirrhosis patients estimated to

account for majority of direct US healthcare cost

burden of NASH1

Moderate to Advanced Fibrosis(FDA Relevant Population)

0

5

10

15

20

25

June 3, 2020

Aldafermin Impacts the Key Drivers of NASH Pathogenesis

6

Liver FatSTEATOSIS

HepaticBALLOONING

Immune ResponseINFLAMMATION FIBROSIS

Resulting Impact on Disease Progression

in the Liver

Insulin Resistance, Toxic Fatty Acids

Metabolic Dysregulation

ALDAFERMIN (NGM282)

Actions on Implicated Disease Drivers

Elevated Bile Acids Exacerbate Injury

Bile AcidDysregulation

Reduce De Novo Lipogenesis Reduce Bile Acid Production

Reduce Toxic Fatty Acids

Insulin Sensitization

FGFR4/KLBFGFR1c/KLB

FGF19 Analog

ImplicatedDisease Drivers

ALDAFERMIN

June 3, 2020

Unlike Many Other Drugs in Development, Aldafermin Targets Fibrosis Reversal and Cirrhosis Prevention in Advanced NASH Patients

7

NASH Patient Segmentation Liver Transplant/

Liver-related Mortality

6.3M 3.4M 2.0M 1.3M

F1 F2 F3 F4

Target Patient Populations

Metabolic Drugs (Many)Competitive Landscape

Drugs with Metabolic and Anti-fibrotic Effect (Limited)

Like Type 2 Diabetes (T2D),

NASH Can Support Multiple

Drug Classes

US Prevalence

Aldafermin • Rapidly reverse fibrosis

• Prevent cirrhosis

• Prevent decompensation, liver events

Other Drugs in Development

Phase 2 data suggest aldafermin may:

June 3, 2020

COHORT 1 COHORT 2 COHORT 3 COHORT 4

StatusCompleted

(Published, The Lancet 2018)Completed

(Presented, EASL 2018)Completed

(Presented, AASLD 2018)

Preliminary Topline Results(More details planned for

EASL 2020)

Duration 24 Weeks

Aldafermin Dose(# Patients)

KEY ENDPOINTS/ Assessment Measures

NASH Phase 2 Program Provides Foundation for Late-Stage Development of Aldafermin

12 Weeks

NON-INVASIVE MEASURES

0.3 mg(23)

1 mg(21)

3 mg(22)

1 mg(28)

1 mg(53)

Placebo(25)

3 mg(27)

Placebo(27)

6 mg(28)

8

HISTOLOGY (Biopsy)

Clinical Data in Presentation

MRI-PDFF: magnetic resonance imaging-estimated proton density fat fraction; ALT: alanine aminotransferase; AST: aspartate aminotransferase; ELF: Enhanced Liver Fibrosis score; PRO-C3: exploratory biomarker of fibrogenesis

STEATOSIS INFLAMMATION BALLOONING FIBROSIS

% Liver Fat Content (LFC)(MRI-PDFF)

ELF/PRO-C3(Biomarkers)

ALT/AST(Biomarkers)

June 3, 2020

Cohort 4: A 24-Week, Double-Blind, Placebo-Controlled Multi-Center Ph2 Study of Aldafermin in Patients with Biopsy-Proven NASH

9

D -28 D1 W24

Placebo SC QD

Aldafermin 1 mg SC QD

MRI-PDFFBiopsy

W6

• Key inclusion criteria include:o Biopsy-confirmed NASH with NAS ≥4 (1 point in each component); stage 2 or 3 liver fibrosis (F2 or F3 by NASH CRN criteria)o Absolute liver fat content (LFC) ≥8% by MRI-PDFF o ALT > 19 IU/L in females, ALT > 30 IU/L in males

• Primary endpoint: change from baseline in absolute LFC (as measured by MRI-PDFF) at W24• Secondary and exploratory endpoints include ALT, AST, biomarkers of fibrosis and effect on liver histology at W24• Over-encapsulated rosuvastatin (ROS 20 mg) started at W2 if low-density lipoprotein cholesterol (LDL-C) rise of 10 mg/dL observed

MRI-PDFFBiopsy

SCREENING ON-TREATMENT STUDY PERIOD FOLLOW-UP

W30W18W12

MRI-PDFF MRI-PDFF MRI-PDFF

Safety population N=78 Aldafermin : placebo (2:1)

Efficacy population N=77 At least one dose and valid post-dose efficacy value

Liver histology population N=72 Valid, non-missing biopsy at baseline and W24

June 3, 2020

Patient Baseline Demographics and Characteristics (Cohort 4 Efficacy Population)

10

ParametersMean (SD)

Placebo (n=25)

Aldafermin 1 mg (n=52)

Age (years) 54.1 (9.7) 53.0 (12.1)

Sex (Male/Female) 9 / 16 27 / 25

Weight (kg) 102.5 (29.7) 100.1 (21.0)

BMI (kg/m2) 36.8 (9.0) 35.8 (6.4)

Waist (cm) 114.3 (17.0) 111.9 (15.4)

Type 2 Diabetes, n (%) 16 (64%) 31 (60%)

NAFLD Activity Score (NAS) 5.4 (1.1) 5.7 (1.1)

Fibrosis stage (F2 / F3)1 13 / 9 27 / 23

Liver Fat Content (% by MRI-PDFF) 18.5 (6.8) 18.0 (5.9)

Alanine aminotransferase, ALT (IU/L) 55.1 (29.6) 73.3 (39.6)

Aspartate aminotransferase, AST (IU/L) 44.3 (23.7) 54.5 (27.4)

HDL-C (mg/dL) 34.5 (16.7) 31.7 (12.5)

LDL-C (mg/dL) 95.0 (31.6) 95.1 (31.0)

Triglycerides (mg/dL) 167.7 (119.2) 194.2 (164.3)

Pro-C3 (ng/mL) 17.1 (7.0) 17.5 (8.4)1 Liver histology population (aldafermin n=50; placebo n=22)

June 3, 2020

Cohort 4: Rapid and Sustained Improvement in Fibrosis

11

Liver Histology Population (n=50 aldafermin vs. n=22 placebo)1 Cohort 4 preliminary topline data; Defined as patients who have an improvement in liver fibrosis by ≥1 stage with no worsening of NASH (no worsening of steatosis, lobular inflammation or hepatocyte ballooning grade) from baseline to W24 (not powered for statistical significance)

Biopsy Reads

• Both baseline and W24 liver biopsies were centrally read by the same NASH-CRN pathologist

• Baseline biopsies were not re-read at end of study

• All biopsies were read blinded to treatment assignment and patient

18%

38%

Placebo 1 mg

Fibrosis Improvement ≥1 Stage with No Worsening of NASH1

at W24

(% of Patients)

Aldafermin1 mg

(n=4)

(n=19)

June 3, 2020

Cohort 4: Additional Benefit in Resolution of NASH

12

Liver Histology Population (n=50 aldafermin vs. n=22 placebo)1 Cohort 4 preliminary topline data; Defined as subjects having a NAS score of 0 or 1 for inflammation and 0 for ballooning, with no worsening of fibrosis (no progression of NASH CRN fibrosis stage) from baseline to W24 (not powered for statistical significance)

9%

24%

Placebo 1 mg

Resolution of NASH without Worsening of Fibrosis1

at W24

(% of Patients)

Aldafermin1 mg

(n=2)

(n=12)

June 3, 2020

Potential Amplification of Fibrosis Improvement and Resolution of NASH with Longer Treatment Duration

13Cohorts 2-3 preliminary data; Cohort 4 preliminary topline data (endpoints not powered for statistical significance); % of patients achieving endpoint

Cohort 4 (W24)1 mg aldafermin vs. placebo

24%

Fibrosis

Resolution of NASH

38%

18%

9%

Aldafermin (n=50)

Placebo (n=22)

Fibrosis Improvement w/o worsening of NASH

Cohort 2 (W12)3 mg aldafermin

Cohort 3 (W12)1 mg aldafermin

42%25%

11%13%

----

----

Resolution of NASH w/o worsening of fibrosis

June 3, 2020

Cohort 4: Statistically Significant Proportion of Patients Achieved Both Fibrosis Improvement AND Resolution of NASH

14

Liver Histology Population (n=50 aldafermin vs. n=22 placebo)1 Cohort 4 preliminary topline data; Defined as patients who have an improvement in liver fibrosis by ≥1 stage with no worsening in NASH AND have a NAS score of 0 or 1 for inflammation and 0 for ballooning without worsening of fibrosis at W24 (not powered for statistical significance)

0%

22%

Placebo 1 mg

Composite Endpoint of Fibrosis Improvement AND Resolution of NASH1 at W24

(% of Patients)

Aldafermin1 mg

* p<0.05

*

(n=11)

June 3, 2020

Cohort 4: Statistically Significant Proportion of Patients Achieved NAS Reduction of ≥ 2 Points

15Liver Histology Population (n=50 aldafermin vs. n=22 placebo)1 Cohort 4 preliminary topline data; endpoint not powered for statistical significance

9%

62%

Placebo 1 mg

Improvement of NAS by ≥ 2 Points without Worsening of Fibrosis1 at W24

(% of Patients)

Aldafermin1 mg

*** p<0.0001

***

(n=31)

(n=2)

Statistically significant improvements in each NAS component of:

• Steatosis

• Lobular Inflammation

• Ballooning

June 3, 2020

Cohort 4 Primary Endpoint Met: Statistically Significant Reduction in Absolute Liver Fat Content (LFC)

16

Cohort 4 (24W)

LFC by MRI-PDFF1

19%15%

Baseline Week 24

1 Cohort 4 preliminary topline data; Relative values are calculated as mean change from baseline

-13%

Placebo Aldafermin 1 mg

Live

r Fa

t C

on

ten

t (%

)

18%

10%

Baseline Week 24

-39%

**P<0.01 vs. placebo

**

• 68% of aldafermin patients achieved ≥ 5% absolute LFC reduction vs. 24% placebo

• 66% of aldafermin patients achieved ≥ 30% relative LFC reduction vs. 29% placebo

• Consistent response on LFC across Cohorts 1-4

June 3, 2020

Cohort 4: Rapid and Sustained Decrease in ALT to Near Normal Levels with Aldafermin

17

****P<0.0001, ***P<0.001 vs. placebo

55 49

Baseline Week 24

-6%73

31

Baseline Week 24

-49%

ALT

(IU

/L)

Placebo Aldafermin 1 mg

Cohort 4 (24W)

ALT (IU/L)1

****

1 Cohort 4 preliminary topline data; Relative values are calculated as mean change from baseline

-80

-60

-40

-20

0

20

40

Placebo (n=25)

Aldafermin 1 mg (n=52)

% C

han

ge in

ALT

fro

m B

asel

ine;

LS

mea

n (

SE)

***

***

*********

******

W2 W4 W6 W12 W24W18W8

Relative Change in ALT

Statistically significant reductions vs. placebo also observed with AST and PRO-C3

June 3, 2020

0

50

100

150

200

0

Placebo (n=25) Aldafermin 1 mg (n=52)

Cohort 4:LDL-C Changes Effectively Managed with Statin Therapy

18

LDL-

C (

mg

/dl)

; mea

n (

SD)

Add Rosuvastatin to Placebo or Aldafermin as Needed(If Needed, Titration at W2, W4, W8)

Cholesterol

FGFR4

C4

Bile Acids

CYP7A1

• Mean LDL-C levels returned to ~77 mg/dL for both placebo and aldafermin arms• Statistically significant reduction in triglycerides observed as early at W2 and sustained through W24

LDL-C elevation is a direct effect of FGF19’s inhibition of the classical bile

acid synthesis pathway

W2 W4 W6 W12 W24W18W8

Cohort 4 preliminary topline dataC4 = 7-hydroxyl-4-cholesten-3-one; CYP7A1: cholesterol 7 alpha-hydroxylase

Aldafermin

June 3, 2020

Cohort 4: Aldafermin Generally Well Tolerated and Most Common Adverse Events Comparable to Placebo

19

Most Common (>10%) Adverse Events

Placebo (N=25)

Aldafermin 1 mg (N=53)

Diarrhea 6 (24.0%) 15 (28.3%)

Headache 9 (36.0%) 7 (13.2%)

Abdominal Distension 3 (12.0%) 7 (13.2%)

Nausea 6 (24.0%) 5 (9.4.%)

Fatigue 4 (16%) 3 (5.7%)

Diabetes Mellitus 5 (20.0%) 2 (3.8%)

Peripheral Edema 3 (12.0%) 2 (3.8%)

TEAE Classification Placebo (N=25) Aldafermin 1 mg (N=53)

Any TEAE 22 (88.0%) 46 (86.8%)

TEAE Leading to Drug Withdrawal 1 (4.0%) 0

Serious Adverse Event (SAE)1 3 (12.0%) 2 (3.8%)

Drug-Related TEAE 11 (44.0%) 27 (50.9%)

TEAE Leading to Death 0 0

Cohort 4 preliminary topline data1 SAEs: Placebo (mental status changes; appendicitis; anxiety); Aldafermin (rectal bleeding; post-biopsy bleeding)

• All SAEs were deemed to be not related to treatment by site investigator

• Pruritus (4% aldafermin vs. 8% placebo)• Injection site bruising (6% aldafermin vs.

0% placebo)

June 3, 2020

Phase 2 Data Supports Aldafermin’s Potential as Differentiated Monotherapy for Treatment of NASH with Established Fibrosis

20Cohorts 2-3 preliminary data; Cohort 4 preliminary topline results; % of patients achieving endpoint

Cohort 4 (W24)1 mg aldafermin vs. placebo

0%Both

9%NAS 2

Fibrosis

Resolution of NASH24%

38%

22%

18%

9%

62%

Aldafermin (n=50)

Placebo (n=22)

Fibrosis Improvement w/o worsening of NASH

Fibrosis Improvement and Resolution of

NASH

NAS Reduction ≥2 Points

w/o worsening of fibrosis

* p<0.05

*

*** p<0.0001

***

Resolution of NASH w/o worsening of fibrosis

Cohort 2 (W12)3 mg aldafermin

Cohort 3 (W12)1 mg aldafermin

42%25%

11%13%

----

----

June 3, 2020

Summary of Aldafermin Cohort 4 Preliminary Topline Results

21

• Meaningful improvements in histology regulatory endpoints: fibrosis improvement, resolution of NASH and the composite endpoint requiring achievement of both

• Aldafermin’s differentiated rapid dual anti-fibrotic and metabolic effect is evidenced by the significant improvements observed as early as two weeks

• Cohort 4 data suggest that the histological effects we observed at 12 weeks are sustained and potentially amplified with extended treatment

• Favorable tolerability profile: most common adverse events occurred with similar frequency in placebo and aldafermin arms

June 3, 2020

Aldafermin Development Plan

22

PHASE 2 – COHORT 4PHASE 2b

(ALPINE 2/3)

PHASE 2b –COMPENSATED CIRRHOTICS

(ALPINE 4) PHASE 3 PROGRAM

StatusComplete Datasetto be Presented

Ongoing Ongoing In Planning

Duration 24 Weeks 24 Weeks 48 weeks TBD

Aldafermin Dose(# Patients)

1 mg(53)

Placebo(25)

0.3 mg, 1 mg, 3 mg(~40 per dose level)

Placebo(~40)

F4

0.3 mg, 1 mg, 3 mg(~40 per dose level)

Placebo(~40)

Dose Level(s) TBD

Placebo

F2/F3F2/F3

June 3, 2020

NGM313 (MK-3655) for the Treatment of NASH and Type 2 Diabetes

23

• Agonistic antibody that selectively activates FGFR1c / KLB to regulate energy metabolism

• Potential to be once-monthly injectable insulin sensitizer for treatment of NASH and T2D

• Completed Phase 1 SAD/MAD study in obese, insulin resistant subjects and Phase 1b study in subjects with NAFLD

• Single dose of NGM313 resulted in significant reductions in liver fat content and improvement in metabolic markers based on preliminary data from a Phase 1b study in obese, insulin resistant subjects with NAFLD after five weeks

• Well-tolerated across Phase 1 and Phase 1b studies

• Merck exercised its option and licensed NGM313 and other FGFR1c/KLB agonists in 4Q18

FGFR2c FGFR3c FGFR4

KLB KLB KLB

FGFR1c

KLBNGM313

FGF21 analogs have demonstrated variable clinical efficacy in metabolic syndrome patients; native

ligand has potential for safety liabilities

June 3, 2020

0%

5%

10%

15%

20%

25%

Baseline Day 36

Significant Reduction in LFC After 5 Weeks Following Single Dose of NGM313 (MK-3655)

24

Absolute LFC (% LS Mean±SE)

Absolute LFCMRI-PDFF

****p<0.0001

****

NGM313

Statistically Significant Improvements In:

• ALT and AST

• Triglycerides

• HDL-C, LDL-C

• PRO-C3

Phase 1b Study in Obese, Insulin Resistant Subjects with NAFLD

-6.3% Absolute-37% Relative

at 5W

Pioglitazone 45 mg

(Positive Control)

• 4.0% absolute (25% relative) LFC reduction at 5W

June 3, 2020

Rapid Reduction in HbA1c Without Hypoglycemia After Single Dose of NGM313 (MK-3655)

25

HbA1c

Reduction in HbA1c observed in insulin-resistant, non-diabetic patients supports

promise of NGM313 to potentially improve glucose control in patients with T2D

5.4

5.5

5.6

5.7

5.8

5.9

6.0

Baseline Day 36

NGM313, 240 mg(n=17)

HbA1c, % (Mean±SE)

5.4

5.5

5.6

5.7

5.8

5.9

6.0

Baseline Day 36

Pioglitazone, 45 mg(n=8)

-0.24%-0.11%

NGM313 increases body weight by 1.6 kg (no edema or fluid retention) vs. 2.4 kg

increase with pioglitazone at day 36

HbA1c, % (Mean±SE)

Phase 1b Study in Obese, Insulin Resistant Subjects with NAFLD

****

* p<0.05; ****p<0.0001

*

June 3, 2020

NGM313 (MK-3655) has Potential to Complement Aldaferminby Targeting NASH Population with T2D

26

NASH Patient Segmentation Liver Transplant/

Liver-related Mortality

6.3M 3.4M 2.0M 1.3M

F1 F2 F3 F4

Target Patient Populations

Metabolic Drugs (Many)Competitive Landscape

Drugs with Metabolic and Anti-fibrotic Effect (Limited)

Like T2D, NASH Can Support

Multiple Drug Classes

US Prevalence

65% of T2D patients have NASH

AldaferminNGM313 (MK-3655)

Complementary Treatments for

NASH

June 3, 2020

OngoingDevelopment

Programs

5

Beyond NASH, an Expansive Pipeline in Other Indications

27

PRODUCTCANDIDATE

PRODUCT DESCRIPTION(DOSING FREQUENCY)

POTENTIALINDICATIONS

STAGE OF DEVELOPMENT

WORLDWIDECOMMERCIAL RIGHTS

Aldafermin(NGM282)

FGF19 Analog(Once Daily)

NASH

NGM313(MK-3655)

FGFR1c/KLB Agonistic Antibody(Once Monthly)

NASH, Type 2 Diabetes

NGM120GFRAL Antagonistic Antibody

(Long Acting)

Cancer,Cancer Anorexia/Cachexia

Syndrome (CACS)

NGM621Complement C3 Inhibitory

Antibody(Long Acting)

Dry AMD / Geographic Atrophy

NGM395GDF15 Analog(Long Acting)

Metabolic

Option

Option

Wholly-OwnedPhase 2b

Phase 1b

Phase 1a/1b

Phase 1

Licensed

FGF19: fibroblast growth factor 19; FGFR1c/KLB: fibroblast growth factor receptor 1c/beta-klotho; GFRAL: glial-cell-derived neurotrophic factor receptor alpha-like; GDF15: growth differentiation factor 15

Wholly-Owned

Phase 1

June 3, 2020

Geographic Atrophy (GA) is an Advanced Form of AMD

28

CNV (Wet AMD)

GA (Dry AMD)

Advanced AMDIntermediate AMD

Larger or more numerous drusen, +/- pigmentary changes

Early AMD

Small or intermediate drusen, +/- pigmentary changes

• GA is the dry form of advanced AMD, characterized by progressive and irreversible loss of photoreceptors, retinal pigment epithelium (RPE) and choriocapillaris

• GA is typically bilateral and lesion enlargement results into irreversible blindness

• GA affects ~5 million people globally and ~ 1 million people in the US

• Currently no approved treatment for GA

CNV = choroidal neovascularizationSources: Fleckenstein et al, Ophthalmology 2018, 125(3): 369-390; Friedman et al, Arch Ophthalmology 2004, 122: 564-572

June 3, 2020 29

Complement Activation is Associated with Development of Advanced AMD

Source: Fritsche et al. Nat Genet 2016

Variants in the complement pathway account for the majority of the known genetic risk for AMD

CFH C9 C2/CFB C3

June 3, 2020

NGM621 Targets Complement C3, Blocking All Three Pathways of Complement Activation

30

C2

C4

Classical Pathway

LectinPathway

AlternativePathway

Factor BFactor D Lampalizumab (Roche)

C3b

C5 C5 convertase

NGM621

C3a

C5a

Inflammation

Opsonization / Phagocytosis

Cell lysis

Membrane AttackComplex (MAC)

Anti-C5 Abs do not block all activities mediated by C3b / C3a

Intervention at C3 may provide superior efficacy for treatment of GA

C3

June 3, 2020

NGM621: A Potent Anti-Complement C3 Antibody

31

• Antibody that has high binding affinity for human C3 (KD < 1 nM)

• Potent inhibition of both classical and alternative pathways of complement activation (IC50 ~ 5-6 nM)

• Potential for QM (monthly) or Q2M (EOM) intravitreal dosing

Anti-C3 Ab reduces vascular leakage in laser injury-induced CNV in mice

Fundus(Day 0)

Complement activation

(Anti-C3d - Day 2)

Vascular leakage (Fluorescein

angiography - Day 7)

Angiogenesis(Isolectin B4 –

Day 7)

Anti-KLH(IVT)

Anti-C3 Ab (IVT)

PBS(IVT)

PEG-40kD(IVT)

Antibody is preferred modality; PEG-40kD exacerbates laser injury-induced CNV in mice

Fundus(Day 0)

Vascular leakage (Fluorescein

angiography - Day 7)

Angiogenesis(Isolectin B4 –

Day 7)

+65% +51%-53% ---41%

June 3, 2020

NGM621 Development

32

• Ongoing Phase 1 open-label single dose and multiple dose study in patients with GA

• Primary objective to evaluate the safety, tolerability and pharmacokinetics of intravitreal injection(s) of single and multiple doses of NGM621

– Estimated enrollment of ~24 patients with GA secondary to AMD

• Study enables a potential Phase 2 POC study in GA

• Favorable tolerability profile observed from 5W GLP toxicology study in monkey

• Program is subject to Merck option to license the program

June 3, 2020

DISCOVERY/PRECLINICAL PHASE 1 PHASE 2 PHASE 3 COMMERCIAL

FUNDING SOURCE($94M UPFRONT + $106M EQUITY INVESTMENT)

DEVELOPMENT/ COMMERCIAL CONTROL

KEYOPT-INDECISIONS

Our Merck Collaboration: Growth-Accelerating Partnership

33

AfterHuman POC

ExclusiveWW License

($20M License Payment)

After Merck ‘Go to Phase 3’

25-50%Cost/Profit

Share

After Phase 3 Data

Option for U.S. Commercial Participation

OR

($50-75M/year in funding1)

1 Merck has committed to provide R&D reimbursement of up to $50 million per year. If our R&D expenses exceed $50 million in a given year, Merck can either reimburse up to an additional $25 million for use in funding IND-enabling or later-staged activities or provide us with the equivalent value in in-kind services for such activities.

June 3, 2020

1Q20 and FY19 Financial Results

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STATEMENT OF OPERATIONS(In thousands)

THREE MONTHS ENDEDMAR 31, 20201

(unaudited)

FULL YEAR ENDEDDEC 31, 2019

(audited)

RELATED PARTY REVENUE $24,364 $103,544

RESEARCH AND DEVELOPMENT EXPENSES

$38,439 $129,253

GENERAL AND ADMINISTRATIVE EXPENSES

$6,595 $23,631

TOTAL OPERATING EXPENSES $45,034 $152,884

NET INCOME ($19,115) ($42,795)

BALANCE SHEETMAR 31, 2020(unaudited)

DEC 31, 2019(audited)

CASH, CASH EQUIVALENTS AND SHORT-TERM MARKETABLE SECURITIES

$328.5M $344.5M

1 See the Company’s Quarterly Report on Form 10-Q for the quarter ended March 31, 2020 for more complete financial information

June 3, 2020

Multiple Potential Value-Driving Catalysts

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Product Candidate Potential Indications Expected Milestones Targeted Timing

ALDAFERMIN NASH F2/F3 Phase 2 Cohort 4 biopsy data 1Q20

ALDAFERMIN NASH F4 ALPINE 4 FPI 1H20

ALDAFERMIN NASH F2/F3 ALPINE 2/3 topline data 1H21

NGM313 (MK-3655)

NASH F2/F3 Phase 2b FPI (Merck) 2H20

NGM120 Cancer/CACS Phase 1a/1b FPI 1Q20

NGM621 Dry AMD/GA Phase 1 safety & tolerability data 2H20

NGM621 Dry AMD/GA Phase 2 FPI 2H20

NGM395 Metabolic Phase 1 FPI 1H20

FPI = first patient in

June 3, 2020

Novel Biology.

Powerful Medicines.

Transformative Impact.

NASDAQ: NGM